Pharmacological ActivationInhibition of the Cannabinoid System Affects Alcohol Withdrawal-Induced Neuronal Hypersensitivity to Excitotoxic Insults 英文参考文献.docVIP

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Pharmacological ActivationInhibition of the Cannabinoid System Affects Alcohol Withdrawal-Induced Neuronal Hypersensitivity to Excitotoxic Insults 英文参考文献.doc

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Pharmacological ActivationInhibition of the Cannabinoid System Affects Alcohol Withdrawal-Induced Neuronal Hypersensitivity to Excitotoxic Insults 英文参考文献

PharmacologicalActivation/Inhibitionofthe CannabinoidSystemAffectsAlcoholWithdrawal-Induced NeuronalHypersensitivitytoExcitotoxicInsults MarinaRubio1,2*,He′le`neVillain1,FabianDocagne1,BenoitD.Roussel1¤,Jose′ AntonioRamos2,3,4 ,Denis Vivien1,JavierFernandez-Ruiz2,3,4,CarineAli1 1INSERM U919 Serine Protease and Pathophysiology of the Neurovascular Unit, UMR CNRS 6232 CINAPS, Caen, France, 2Departamento de Bioqu?′mica y Biolog?′a Molecular, Instituto Universitario de Investigacio′n en Neuroqu?′mica, Universidad Complutense, Madrid, Spain, 3Centro de Investigacio′n Biome′dica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Universidad Complutense, Madrid, Spain, 4Instituto Ramo′n y Cajal de Investigacio′n Sanitaria (IRYCIS), Facultad de Medicina,UniversidadComplutense,Madrid,Spain Abstract Cessationofchronicethanolconsumptioncanincreasethesensitivityofthebraintoexcitotoxicdamages.Cannabinoids have been proposed as neuroprotectants in different models of neuronal injury, but their effect have never been investigated in a context of excitotoxicity after alcohol cessation. Here we examined the effects of the pharmacological activation/inhibition of the endocannabinoid system in an in vitro model of chronic ethanol exposure and withdrawal followedbyanexcitotoxicchallenge.EthanolwithdrawalincreasedN-methyl-D-aspartate(NMDA)-evokedneuronaldeath, probably by altering the ratio between GluN2A and GluN2B NMDA receptor subunits. The stimulation of the endocannabinoid system with the cannabinoid agonist HU-210 decreased NMDA-induced neuronal death exclusively in ethanol-withdrawn neurons. This neuroprotection could be explained by a decrease in NMDA-stimulated calcium influx after the administration of HU-210, found exclusively in ethanol-withdrawn neurons. By contrast, the inhibition of the cannabinoidsystemwiththeCB1receptorantagonistrimonabant(SR141716)duringethanolwithdrawalincreaseddeathof ethanol-withdrawnneuronswithoutanymodificationofNMDA-stimulatedcalci